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Nephrology Dialysis Transplantation, Vol 13, Issue 90008 20-25, Copyright © 1998 by Oxford University Press

ORIGINAL ARTICLES

Molecular biology of diabetic glomerulosclerosis

D Del Prete, F Anglani, M Ceol, A D'Angelo, M Forino, D Vianello, B Baggio and G Gambaro
Instituto di Medicina Interna, Divisione di Nefrologia 1, Policlinico Universitario, via Giustiniani 2, 35128 Padova, Italy; Corresponding author

Diabetic nephropathy is one of the leading causes of renal failure in Western countries, where diabetic patients account for nearly half of all patients on haemodialysis. Progressive expansion of the mesangial matrix, and thickening of the glomerular and tubular basement membranes without signs of major cell proliferation are hallmarks of human and experimental diabetic nephropathy. These lesions eventually lead to glomerular fibrosis, a central pathological feature in many human acute and chronic kidney diseases, which progressively destroys the renal filtration unit, and may finally cause renal failure. Indeed, structure-function relationship studies have shown that mesangial matrix expansion is strongly related to the clinical manifestation of diabetic nephropathy.Key words: angiotensin II; collagen IV; metalloproteinases; transforming growth factor-{beta} vascular endothelial growth factor
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